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Parasite Immunol ; 31(12): 741-9, 2009 Dec.
Article in English | MEDLINE | ID: mdl-19891612

ABSTRACT

Protection against Mesocestoides corti, a cestode that invades vital organs, is dependent on the production of IL-4, as IL-4(-/-) mice were found to have higher parasite burdens when compared with wild-type mice. The goal of this study was to investigate the role of IL-4 in immunity to M. corti, focusing on the immunological profile and on potential mediators of pathology. IL-4(-/-) mice infected with M. corti showed 100% mortality by 32 days, whereas wild-type mice survived for approximately 1 year. Parasite burdens were significantly increased in the liver, peritoneal, and thoracic cavities of IL-4(-/-) mice, associated with impaired recruitment of inflammatory cells and a reduction in monocytes and macrophages. IL-5 production by splenocytes and expression in liver tissue was decreased in infected IL-4(-/-) mice compared with wild-type mice. In contrast, IL-4(-/-) mice produced increased amounts of IFNgamma and TNFalpha. Alternatively activated macrophages were a major feature of liver granulomas in wild-type mice evidenced by Arginase I expression, while livers from infected IL-4(-/-) mice showed impaired alternative macrophage activation without increased classical macrophage activation. Thus, lethality during M. corti infection of IL-4(-/-) mice is associated with decreased Th2 cytokines, increased Th1 cytokines and impairment of alternatively activated macrophages.


Subject(s)
Cestode Infections/immunology , Host-Parasite Interactions/physiology , Interleukin-4/immunology , Macrophages/immunology , Mesocestoides , Th2 Cells/immunology , Animals , Cestode Infections/metabolism , Cestode Infections/parasitology , Host-Parasite Interactions/immunology , Interferon-gamma/biosynthesis , Interleukin-4/genetics , Interleukin-5/biosynthesis , Liver/immunology , Liver/parasitology , Macrophage Activation , Mice , Mice, Inbred BALB C , Mice, Knockout , Spleen/immunology , Spleen/metabolism , Th2 Cells/metabolism , Tumor Necrosis Factor-alpha/biosynthesis
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